TAB3, short for TGF-β-activated kinase 1 (MAP3K7) binding protein 3, is an essential component in multiple biological pathways. It interacts with TAK1 and is crucial for the activation of NF-κB and MAPKs, which are involved in regulating a wide range of physiological and pathological processes, including inflammation, cell apoptosis, and proliferation [2].

In conditional knockout mouse models where METTL3, an N6-adenosine-methyltransferase-like 3, was knocked out in kidneys, cisplatin-and ischemic/reperfusion-induced renal injury and inflammation were attenuated. It was found that METTL3 promoted m6A modifications of TAB3, enhancing its stability via IGF2BP2-dependent mechanisms. This indicates that TAB3 is involved in renal injury and inflammation processes [1].

In TAB3 knockout mouse models, more cardiomyocytes apoptosis, decreased cardiomyocyte proliferation, and weaker angiogenesis were observed both in vitro and in vivo, along with worse cardiac function and enlarged scar formation in the heart, suggesting TAB3 plays a protective role in ischemic heart disease [3].

In conclusion, TAB3 is vital in regulating processes related to inflammation, cell apoptosis, and proliferation. Gene knockout models, especially in the context of renal and cardiac diseases, have revealed its significance in these disease areas, providing insights into potential therapeutic targets for conditions like acute kidney injury and ischemic heart disease.